Type 2 diabetes (T2D) is a complex disease driven by a combination of genetic and environmental factors. In recent years,
several lines of evidence suggest that circadian disruption and sleep loss contribute to disease pathogenesis. Epidemiologic
studies indicate that shift work is associated with an increased risk of T2D (1,2). Shift work is a prime example of circadian disruption, altering the timing of light exposure, meals, activity, and sleep.
In many ways, the shift workers serve as early indicators, or “canaries in a coal mine,” of the long-term consequences of
the circadian disruption experienced by a much broader segment of the population. A number of studies have concluded that
genetic variation in melatonin receptors (notably expressed in pancreatic β-cells) is associated with impaired insulin secretion
and increased risk for T2D (3,4). Similarly, genetic variation in the genes responsible for the generation of circadian rhythms has been linked to metabolic,
endocrine, and behavioral changes that could push a patient toward development of T2D (5,6). This type of population study has been complimented by laboratory studies demonstrating that short duration of sleep adversely
impacts glucose tolerance (7,8). More recently, laboratory studies where healthy participants were exposed to circadian misalignment using a forced desynchrony
protocol provided causative evidence for a deleterious impact on diabetes risk and cardiovascular function (9,10). Sleep and circadian disruption have even been found to hinder the …